Long term 25-hydroxyvitamin D3 therapy in postmenopausal osteoporosis

Demonstration of responsive and nonresponsive subgroups

J. E. Zerwekh, K. Sakhaee, K. Glass, C. Y C Pak

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Previous studies from our laboratory have demonstrated that 25-hydroxyvitamin D3 (25-OHD3) therapy is effective in raising the impaired intestinal calcium absorption (α) associated with postmenopausal osteoporosis. In the present study we have assessed the effects of long term 25-OHD3 therapy (50 μg/day; mean treatment period, 1.3 yr) in 12 women with postmenopausal osteoporosis (mean age, 62.5 yr). Our results indicate that there was a significant increase in α for the group during therapy. However, we found that the patients could be divided into 2 groups based upon their ability to raise α in response to 25-OHD3 therapy. In those who responded (n = 7), α increased from 0.36 ± 0.05 to 0.49 ± 0.8 (±SD; P < 0.005) while no significant change was observed for the nonresponders (0.44 ± 0.03 to 0.48 ± 0.07). During therapy, there were significant increases in serum 25-OHD and 24,25-dihydroxyvitamin D [24,25-(OH)2D] for both groups. Serum 1,25-(OH)2D significantly increased in the responders (21 ± 8 to 39 ± 13 pg/ml; P < 0.01), but not in nonresponders (25 ± 11 to 28 ± 8 pg/ml). Between group comparisons for responders vs. nonresponders before therapy disclosed significant reductions in 24,25-(OH)2D (0.4 ± 0.3 vs. 2.2 ± 0.8 ng/ml; P < 0.005) and α (0.36 ± 0.05 vs. 0.44 ± 0.03: P < 0.01). During therapy, there were no significant differences in any parameter between the two groups, except for serum 1.25-(OH)2D which was significantly higher in the responders (39 ± 13 vs. 28 ± 8 pg/ml; P < 0.05). These data would suggest that in postmenopausal osteoporosis, the ability to raise α in response to 25-OHD3 therapy is due in part to increases in serum 1,25-(OH)2D during therapy. This suggests that in some patients with postmenopausal osteoporosis, renal 25-OHD3-1α-hydroxylase may be impaired.

Original languageEnglish (US)
Pages (from-to)410-413
Number of pages4
JournalJournal of Clinical Endocrinology and Metabolism
Volume56
Issue number2
StatePublished - 1983

Fingerprint

Calcifediol
Postmenopausal Osteoporosis
Dihydroxycholecalciferols
Mixed Function Oxygenases
Demonstrations
Calcium
Aptitude
Therapeutics
Serum
Intestinal Absorption
Group Psychotherapy
Kidney

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

@article{1df59f04a5fa4c55a5e3389a3b7690b1,
title = "Long term 25-hydroxyvitamin D3 therapy in postmenopausal osteoporosis: Demonstration of responsive and nonresponsive subgroups",
abstract = "Previous studies from our laboratory have demonstrated that 25-hydroxyvitamin D3 (25-OHD3) therapy is effective in raising the impaired intestinal calcium absorption (α) associated with postmenopausal osteoporosis. In the present study we have assessed the effects of long term 25-OHD3 therapy (50 μg/day; mean treatment period, 1.3 yr) in 12 women with postmenopausal osteoporosis (mean age, 62.5 yr). Our results indicate that there was a significant increase in α for the group during therapy. However, we found that the patients could be divided into 2 groups based upon their ability to raise α in response to 25-OHD3 therapy. In those who responded (n = 7), α increased from 0.36 ± 0.05 to 0.49 ± 0.8 (±SD; P < 0.005) while no significant change was observed for the nonresponders (0.44 ± 0.03 to 0.48 ± 0.07). During therapy, there were significant increases in serum 25-OHD and 24,25-dihydroxyvitamin D [24,25-(OH)2D] for both groups. Serum 1,25-(OH)2D significantly increased in the responders (21 ± 8 to 39 ± 13 pg/ml; P < 0.01), but not in nonresponders (25 ± 11 to 28 ± 8 pg/ml). Between group comparisons for responders vs. nonresponders before therapy disclosed significant reductions in 24,25-(OH)2D (0.4 ± 0.3 vs. 2.2 ± 0.8 ng/ml; P < 0.005) and α (0.36 ± 0.05 vs. 0.44 ± 0.03: P < 0.01). During therapy, there were no significant differences in any parameter between the two groups, except for serum 1.25-(OH)2D which was significantly higher in the responders (39 ± 13 vs. 28 ± 8 pg/ml; P < 0.05). These data would suggest that in postmenopausal osteoporosis, the ability to raise α in response to 25-OHD3 therapy is due in part to increases in serum 1,25-(OH)2D during therapy. This suggests that in some patients with postmenopausal osteoporosis, renal 25-OHD3-1α-hydroxylase may be impaired.",
author = "Zerwekh, {J. E.} and K. Sakhaee and K. Glass and Pak, {C. Y C}",
year = "1983",
language = "English (US)",
volume = "56",
pages = "410--413",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "2",

}

TY - JOUR

T1 - Long term 25-hydroxyvitamin D3 therapy in postmenopausal osteoporosis

T2 - Demonstration of responsive and nonresponsive subgroups

AU - Zerwekh, J. E.

AU - Sakhaee, K.

AU - Glass, K.

AU - Pak, C. Y C

PY - 1983

Y1 - 1983

N2 - Previous studies from our laboratory have demonstrated that 25-hydroxyvitamin D3 (25-OHD3) therapy is effective in raising the impaired intestinal calcium absorption (α) associated with postmenopausal osteoporosis. In the present study we have assessed the effects of long term 25-OHD3 therapy (50 μg/day; mean treatment period, 1.3 yr) in 12 women with postmenopausal osteoporosis (mean age, 62.5 yr). Our results indicate that there was a significant increase in α for the group during therapy. However, we found that the patients could be divided into 2 groups based upon their ability to raise α in response to 25-OHD3 therapy. In those who responded (n = 7), α increased from 0.36 ± 0.05 to 0.49 ± 0.8 (±SD; P < 0.005) while no significant change was observed for the nonresponders (0.44 ± 0.03 to 0.48 ± 0.07). During therapy, there were significant increases in serum 25-OHD and 24,25-dihydroxyvitamin D [24,25-(OH)2D] for both groups. Serum 1,25-(OH)2D significantly increased in the responders (21 ± 8 to 39 ± 13 pg/ml; P < 0.01), but not in nonresponders (25 ± 11 to 28 ± 8 pg/ml). Between group comparisons for responders vs. nonresponders before therapy disclosed significant reductions in 24,25-(OH)2D (0.4 ± 0.3 vs. 2.2 ± 0.8 ng/ml; P < 0.005) and α (0.36 ± 0.05 vs. 0.44 ± 0.03: P < 0.01). During therapy, there were no significant differences in any parameter between the two groups, except for serum 1.25-(OH)2D which was significantly higher in the responders (39 ± 13 vs. 28 ± 8 pg/ml; P < 0.05). These data would suggest that in postmenopausal osteoporosis, the ability to raise α in response to 25-OHD3 therapy is due in part to increases in serum 1,25-(OH)2D during therapy. This suggests that in some patients with postmenopausal osteoporosis, renal 25-OHD3-1α-hydroxylase may be impaired.

AB - Previous studies from our laboratory have demonstrated that 25-hydroxyvitamin D3 (25-OHD3) therapy is effective in raising the impaired intestinal calcium absorption (α) associated with postmenopausal osteoporosis. In the present study we have assessed the effects of long term 25-OHD3 therapy (50 μg/day; mean treatment period, 1.3 yr) in 12 women with postmenopausal osteoporosis (mean age, 62.5 yr). Our results indicate that there was a significant increase in α for the group during therapy. However, we found that the patients could be divided into 2 groups based upon their ability to raise α in response to 25-OHD3 therapy. In those who responded (n = 7), α increased from 0.36 ± 0.05 to 0.49 ± 0.8 (±SD; P < 0.005) while no significant change was observed for the nonresponders (0.44 ± 0.03 to 0.48 ± 0.07). During therapy, there were significant increases in serum 25-OHD and 24,25-dihydroxyvitamin D [24,25-(OH)2D] for both groups. Serum 1,25-(OH)2D significantly increased in the responders (21 ± 8 to 39 ± 13 pg/ml; P < 0.01), but not in nonresponders (25 ± 11 to 28 ± 8 pg/ml). Between group comparisons for responders vs. nonresponders before therapy disclosed significant reductions in 24,25-(OH)2D (0.4 ± 0.3 vs. 2.2 ± 0.8 ng/ml; P < 0.005) and α (0.36 ± 0.05 vs. 0.44 ± 0.03: P < 0.01). During therapy, there were no significant differences in any parameter between the two groups, except for serum 1.25-(OH)2D which was significantly higher in the responders (39 ± 13 vs. 28 ± 8 pg/ml; P < 0.05). These data would suggest that in postmenopausal osteoporosis, the ability to raise α in response to 25-OHD3 therapy is due in part to increases in serum 1,25-(OH)2D during therapy. This suggests that in some patients with postmenopausal osteoporosis, renal 25-OHD3-1α-hydroxylase may be impaired.

UR - http://www.scopus.com/inward/record.url?scp=0020678725&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020678725&partnerID=8YFLogxK

M3 - Article

VL - 56

SP - 410

EP - 413

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 2

ER -